1 host defenses adaptive innate. 2 defense barriers physical chemical cellular defenses inflammation...
TRANSCRIPT
1
Host Defenses
Adaptive
Innate
2
Defense Barriers
Physical
Chemical
Cellular defenses
Inflammation
Fever
Molecular defenses
3
Physical Barriers
Skin– Stratified– Close intercellular junctions– Waterproof, dead cells
Mucous membranes– Simple epithelium– Mucus layer
4
Chemical Barriers
Salt
pH
Lysozyme
Transferrin
Lactoferrin
Defensins
5
Cellular Defenses - Granulocytes
Basophils/Mast cells
Eosinophils
Neutrophils
Dendritic cells
6
Cellular Defenses — Agranulocytes
Monocytes Lymphocytes
7
Phagocytosis Cells Involved:
Steps involved– Chemotaxis
• Toll-like receptors on phagocytes (TLRs)• Recognition of microbial surface molecules• Cytokines, complement substances from damaged host cells
– Adherence• Capsules, M proteins reduce this• Complement proteins enhance this
– Ingestion• Formation of _______________
– Digestion• __________ + _______________ = _______________________
– Formation inhibited by P. falciparum• Enzymes and reactive oxides damage microbes
– Capsule protects microbes like Y. pestis– Staph. Strep. release WBC degrading toxins - Leukocidins
8
Characteristics of Inflammation
Cardinal signs:
Acute Inflammation
Chronic Inflammation– Continuous pus formation– Healing never achieved– Granulomatous tissue (gummas, tubercles, lepromas)– Steroidal anti-inflammatories can release microbes from
granulomas
9
Fever
Exogenous Pyrogens
Endogenous Pyrogens
Benefits/Risks– Too hot for some microbes to grow, toxins may
inactivate– Increase in interferon, phagocytosis, immune resonse,
transferrin, lysosomal activity– Patients will rest– Convulsions, cardiac stress, dehydration may occur
with v. high fevers Leukocyte Endogenous Mediator
10
Interferons (IFN)
Type I
Type II
11
Complement Proteins
Serum proteins (10% by weight)
Activated by– Ag/Ab complexes
(___________-)– Ag on pathogen
surface (____________)
Activation leads to
Rapid effects, before immune cells are activated, esp. alternate pathway